This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This proposal entitled "The role of protein malnutrition on circadian physiology of C57BL/6J mouse dams and their offspring" aims to investigate the underlying role of desynchronized circadian rhythms after exposure of female mice to a protein deficient diet and the outcome of this expose to the circadian phenotype of the offspring. The process by which the intra-uterine environment plays a role in establishing the health of the offspring has been termed "fetal programming". Maternal under-nutrition as well as other factors can lead to offspring that display inter-uterine growth retardation (IUGR) and have reduced birth weight. Through unknown mechanisms, maternal malnutrition in rodents has been associated with altered responses to hormones regulating food intake and energy expenditure leading to lifelong hyperphagia and an obesity that is associated with a diabetic phenotype. Prenatal exposure to a low protein diet is a commonly used model mimicking fetal under-nutrition, and when administered to rat dams, results in offspring exhibiting signs of Type II diabetes.